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FIGURE 2 Schematic diagram of the experimental setup. 7 ; test compartment; 2 ; sucrose gap; 13 ; KCl compartment; M microelectrodes; S specimen of sinus node tissue.

FIG. 2. Recovery from NH, Cl-mediated alkalinization in the presenceof bumetanide inHEPES-BSS. VSMC were grown and pHi measured as in Fig. 1. 100 p~ bumetanide was added immediately prior to alkalinization with NH4C1at the artifact 26 s ; . ang 11-treated cells; B , control cells. treated cells 100 nM for 24 h ; had a higher rate of recovery 13.86 f 1.87 mmol of H + min liter of cells ; than controlcells 6.68 f 1.01 mmol of H + min liter of cells, n 4; p 0.05 ; . T h increased recovery was not due to a difference in intracellular buffering capacities which were 32.78 f 6.89 mmol of H + unit and 32.15 f 4.72 mmol of H + unit n 4 ; for ang11-treated and controlcells, respectively p 0.1 ; . T o determine if the cotransporter the mechanism was responsible for the ang 11-induced increasein recovery rate observed following NH4C1-induced alkalinization, we studied the effects of bumetanide, a pharmacological inhibitor of the Na K 2C1 cotransporter, on the alkaline recovery rate. Bumetanide 100 ; -sensitiverecovery was significantly increased in ang 11-treated VSMC 9.16 & 1.90 mmol of H + min liter of cells ; compared to control cells 2.11 f 1.46 mmol of H + min liter of cells ; , a 334% increase n 2, p 0.05; Fig. 2 ; . * To define further the effects of ang 11-induced hypertrophy on Na K 2Clcotransportin VSMC, we studiedbumetanidesensitive ffiRb uptake. shown in Table I, there was a 70% As increase in the bumetanide-sensitive 86Rb uptake in ang IItreated 3.97 f 0.03 mmol of K + min liter of cells, n 3 ; versus control cells 2.33 f 0.06 mmol of K + min liter of cells, n 3 ; . Thus, as evidenced by both increased bumetanidesensitive pHi recovery and ffiRb uptake, Na K 2Cl cotransport was increased in ang11-treated, hypertrophied VSMC. To characterize further the mechanism NH4 + transport for in VSMC, we used N CH3 ; 4 + , which, due to steric hindrance, would be less likely to be transported. Therewas no difference in peak pHi values achieved with NH&l 7.89 + . 0.02, n 6 ; or N CHJ4Cl 7.84 f 0.05, n 2; p 0.1 ; . As shown in Fig. The standard errors of alldrug-sensitive transport rates are calculated as S.E. [ S.E., ; ' + S.E.Z ; ']''', resulting in multiplication of the statistical errors. Supreme Court criticized part of the qualified immunity analysis in Hill, but not Hill's analysis of what constitutes a serious medical need of prisoners ." ; . Under this standard, Plaintiff s claims against Defendant must fail . To begin, the Court will address the period of time following Plaintiff' s falls in February 2002 . To the extent Plaintiff avers that his treatment for injuries resulting from his falls was deficient, he has produced no evidence to substantiate such a claim . Indeed, the evidence shows that Plaintiff received immediate and constant medical attention in the months immediately following his falls. Plaintiff received X-rays and medications, and reports in his own verified complaint that Defendant interviewed him weekly and regularly checked on Plaintiff's medical status . Doc . no. 1, p. 7 ; . Indeed, Plaintiff's chief complaint regarding the period following his falls is that Defendant refused to prescribe stronger pain medication . Given these facts , there is nothing from which to suppose that Defendant was deliberately indifferent to Plaintiff's post-fall medical needs . Plaintiff does not aver that he did not receive medical attention following his falls , but rather that Defendant acted with deliberate indifference when he did not pursue Plaintiff 's preferred course of treatment--namely, the presc ription of stronger pain medication . The burden ofproving deliberate indifference cannot be met simply by arguing that an inmate wanted a different type of treatment . Hamm v. DeKalb County, 774 F .2d 1567, 1575 Cir . 1985 ; "Where a p risoner has received . medical attention and the dispute is over the adequacy oftreat cent , federal courts are generally reluctant to second guess medical judgments . Id. citation omi tted . The Court underscores here that "not every claim by a prisoner that he has not received adequate medical treatment states a violation of the Eighth Amendment." West, 320 F.3d at.

FIG. 8. Km for Na A ; , Rb and Ki for bumetanide D ; . The concentrations of Na and Cl were as described in Figs. 6 and 7. Concentrations of Rb were 0.1, 0.7, 1.3, and 20 mM, and concentrations of bumetanide were 0, 0.02, 0.05, 0.1, and 2 M. To determine Ki for bumetanide inhibition, the cells were preincubated for 15 min at various inhibitor concentrations in 20 mM medium 2, 6 ; . The Km or Ki from each individual experiment was determined using a single binding site model for Na , Rb , and bumetanide, and a two binding site model Hill coefficient 2 ; for Cl . The numbers of individual concentration curves used to generate each bar were 9 32. Fill the eluent container with degassed, high-purity, deionized water. Turn on the gradient pump to begin the flow of eluent through the system. If the system backpressure is below 14 MPa 2000 psi ; , a length of yellow PEEK 0.003-in. 0.075-mm ; tubing should be added between the outlet of the degas assembly in the EG50 and the inlet of the injection valve. For optimal EG50 performance, maintain a system backpressure of 15.216.6 MPa 22002400 psi ; . Confirm that there are no leaks in the chromatographic pathway. For more information, see the Operator's Manual for the EG50 Eluent Generator System Document Number 031908 ; . Using Chromeleon, turn on the EG50 to deliver the highest eluent concentration required by the method. Allow the LC30 oven to stabilize at 30 C. Determine the status of the system by measuring the short-term noise. In a representative 1-min level portion of the chromatogram, a peak-to-peak measurement should be less than 10 nS. It may take 12 h or more for the system to equilibrate to a stable background conductivity for trace analysis. We recommend running the system overnight to equilibrate for use the following day. For method 2, select "Concentrator" as the "Injection Type" on the front panel of the AS40 Autosampler. This selection configures the autosampler to load at 1 mL min against a concentrator backpressure between 345 and 690 kPa 50 and 100 psi ; . The "Bleed On" will be set automatically when the "Injection Type" is set to "Concentrator". This setting prevents air from accidentally being forced through the concentrator column and ensures that an accurate, reproducible volume is loaded for each injection. Select the "Proportional" sampling mode to deliver a sample aliquot equal to the fill volume of the 5-mL vial. For more information on the operation of the autosampler, see the Operator's Manual for the AS40 Automated Sampler Document Number 034970 ; . 4 and buspirone.

50%, as reported here, the HCMV infection may bias the protein synthetic machinery in favor of viral proteins. Finally, there is the possibility of virally mediated posttranslational modification of the NKCC. It is possible that a virally induced proteolytic activity might result in the reduction of NKCC activity and protein expression we observed. Cell swelling is also known to inhibit the cotransporter e.g., Ref. 13 ; , and might be considered as a reason for the loss of NKCC activity following HCMV infection. However, we show that this loss is already quite prominent by 24 h PE, well before the cell volume increases 1, 2 ; . What is basis of the increased [Cl ]i caused by HCMV infection? Maglova et al. 21 ; reported that 72 h PE, HCMV infection increased the [Cl ]i of MRC-5 cells bathed in HCO3 saline by 37 mM. When the cells were bathed in HEPES saline, the [Cl ]i still increased by 27 mM. Our present results confirm this latter increase of [Cl ]i after 72 h of HCMV infection and extend it by showing that the increase has already begun within 24 h of the infection, when the [Cl ]i had increased from 53.4 mM to 65.2 mM, an increase of 12 mM. The present results clearly show that the nonHCO3 -dependent increase of [Cl ]i noted by Maglova et al. 21 ; cannot be caused by enhanced NKCC activity in the HCMV-infected cells. Nor do the present results comparing the effects on net Cl uptake of bumetanide treatment and Na -free treatment see Fig. 5 and Table 2 ; point to an enhanced Na -Cl cotransport process as being the cause for the increased [Cl ]i. We have suggested 21 ; that the HCMV-infected cells might be substantially depolarized relative to the mock-infected cells. Even in the absence of any active uptake of Cl , membrane depolarization coupled with a voltagesensitive pathway for Cl transmembrane movement would result in an increase of [Cl ]i. Therefore, the higher [Cl ]i may be the combined result of an enhanced Cl HCO3 exchanger activity and a depolarized membrane potential. HCMV reduces NKCC activity while upregulating Na H exchanger and Cl HCO3 exchanger activities. Why does the virus downregulate the NKCC at the same time it is upregulating the Na H exchanger and the Cl HCO3 exchanger activities 21 ; ? Both mechanisms import Na and Cl , and it is reasonable to assume that most of the imported Na is exchanged for K via the simultaneously upregulated Na pump Fig. 7; see Refs. 2, 12, 27 ; . Hence, both mechanisms would presumably result in the net uptake of isosmotic K Na Cl solution. An obvious difference between the two approaches is that the NKCC mechanism directly imports K in addition to the K exchanged for Na , leading to the possibility that this mechanism would result in a higher [K ]i than the combined Na H exchanger and Cl HCO3 exchanger mechanism. However, as long as the Na pump exchanges most of the imported Na for K , this difference is unlikely to be important.

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